ArticleFrontiers in physiology2023
Maintenance of subsynaptic myonuclei number is not driven by neural input.
Article in Frontiers in physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Disrupted Motor Neuron and Neuromuscular Junction Development in an Albino Mice Model of Infantile Nystagmus.Investigative ophthalmology & visual science · 2025Article
- Aging in the Skeletal Muscle Revealed by Molecular Immunohistochemical Imaging.International journal of molecular sciences · 2025Review
- SMN depletion impairs skeletal muscle formation and maturation in a mouse model of SMA.Human molecular genetics · 2025Article
- Postsynaptic BMP signaling regulates myonuclear properties in Drosophila larval muscles.The Journal of cell biology · 2025Article
- Differential evaluation of neuromuscular injuries to understand re-innervation at the neuromuscular junction.Experimental neurology · 2024Article
- Postsynaptic BMP signaling regulates myonuclear properties inbioRxiv : the preprint server for biology · 2024Article
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Authors and funding
3 authors.
Funding
Abstract
The development and maintenance of neuromuscular junctions (NMJ) are supported by a specialized population of myonuclei that are referred to as the subsynaptic myonuclei (SSM). The relationship between the number of SSM and the integrity of the NMJ as well as the impact of a loss of innervation on SSM remain unclear. This study aimed to clarify these associations by simultaneously analyzing SSM counts and NMJ innervation status in three distinct mouse models of acute and chronic NMJ disruption. SSM were identified using fluorescent immunohistochemistry for Nesprin1 expression, which is highly enriched in SSM, along with anatomical location beneath the muscle fiber motor endplate. Acute denervation, induced by surgical nerve transection, did not affect SSM number after 7 days. Additionally, no significant changes in SSM number were observed during normal aging or in mice with chronic oxidative stress (
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